8 Best Yoga Asanas To Treat Migraine


Neuroplastic pain changes to the brain don’t happen in isolation. Rather, they are heavily influenced by what is perceived by the body through chemical inflammatory mediators.

Fascinating research has shown that the way genes are expressed can have a big impact on chronic pain, even though there are no changes in the actual DNA sequences. This is known as epigenetics, the study of how certain genes are “turned on” or “turned off,” sometimes with negative results.

Certain inflammatory mediators can lead to epigenetic changes in the way DNA is expressed or “used” by the body. As a result, environmental factors like stress, nutrition, toxins, medications, and exercise can have a potentially significant impact on a person’s pain experience, for better or for worse.

Preliminary studies suggest chronic pain states are associated with widespread epigenetic changes in the brain. For example, in the prefrontal cortex, the amount of change correlates with the severity of the pain. Learning more about the ways in which pain influences epigenetics will help us better understand how the “pain brain” is developed and how it can be healed.

Zeroing In on the Brain Changes

Remember Heather, the 32-year-old woman who developed chronic pain after smashing into a fence while playing softball? My guess is that her brain had been radically altered.

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There were undoubtedly changes within Heather’s somatosensory cortex, the center for receiving sensory information from the body that has a detailed “map” telling the brain where the information is coming from Imagine cutting a short length of ribbon, placing one end on your left, ear and running it over the top of your head to your right ear. This will give you a rough idea of where the somatosensory cortex lies: under the ribbon. The cortex works well until chronic pain sets in, when it becomes altered. Changes in the somatosensory cortex lead to problems in distinguishing where sensory information is coming from, and produce body image distortions that make a painful body part seem larger than it actually is. Changes to the cortex might lead to a dissociation from, or a neglect of, the painful body part, leading the person to ignore a painful body part or avoid using it. This was certainly true in Heather’s case. Not only was she so fearful of hitting her injured head that she had nightmares about it, but she didn’t want to be touched at all.

Meanwhile the glial cells, which are intertwined with and nurture the brain’s neurons, can have their own response to ongoing pain. These “helper cells” normally secrete substances that regulate the flow of information from neuron to neuron, increasing or dampening the flow as necessary. But when neurons start firing off lots of pain signals, the glial cells may interpret this as meaning the neurons have been damaged. Attempting to fix the problem, the glial cells secrete substances that allow nerve signals to travel more freely, as well as substances that encourage inflammation, part of the body’s healing process. The glial cells are well-intended, but the result of their action is to keep the pain signals flowing and lock the chronic pain patient’s brain in a constant state of alarm—which leads to more pain. New research supports the idea that chronic pain may be related to disturbances in the way glial cells and neurons interact,7 and that disturbed glial cells may keep the pain alive.

It’s not just the parts of the brain handling the physical sensations of pain that are altered by chronic pain; so are the areas dealing with the way that pain is understood. As Heather, and everyone else in chronic pain knows, the pain is not just a physical phenomenon. Instead, it is linked to feelings of fear, anxiety, depression, and more. Pain is no longer a solo sensation; it is always accompanied by unhappy feelings: thus Heather’s depression, anxiety, and irritability.

There is a special part of the brain where pain is given emotional significance, linking it to fear, depression, and other negative feelings. When Heather first ran into the fence, the feeling of pain passed through this part of her brain, called the amygdala, which consists of two almond-shaped areas deep within the organ, one on the right side and one on the left. At first, her pain was linked to feelings of fear and danger: Something bad has happened, get away, get help! Over time, however, as the pain continued, the behavior of Heather’s amygdala evolved and it began linking negative emotions to the ongoing pain, leading to personality changes. The pain was initially linked to a feeling of fear, but then it became linked to anger, depression, and other negative feelings. That was why Heather was so angry and grouchy, and snapped at her husband and kids all the time.

The amygdala works closely with an area of the brain called the prefrontal cortex, which sits right behind the forehead and handles decision making, social interaction, and planning. Special brain scans have shown that the part of the prefrontal cortex where decision making occurs can shrink in size when chronic pain settles in, explaining why it becomes so difficult to think things through. It’s not just that the feeling of pain is so darn distracting: The pain actually makes it harder to think things through and make a decision. Since the prefrontal cortex is our “executive director” and “lead decision maker,” changes to this part of the brain may explain changes in Heather’s behavior, like avoiding interaction with others and not wanting to do anything but sit.

Close to the amygdala is an area of the brain called the hippocampus, which regulates learning and memory. Changes to this area can make it difficult to remember and learn new things. Like the prefrontal cortex, the hippocampus literally shrinks in people suffering from chronic pain,8 which helps explain why Heather was constantly taking notes at work and forgetting what had just been said. It was impossible for her to remember things the way she had before her injury.

Imagine those pain sensations emanating from Heather’s head, neck, and shoulders, triggering feelings of anger and fear, dampening her ability to make decisions and remember, and turning her into “a totally different person.” That’s all bad enough, but there’s more. The continuing pain also changes the way she responds to stress. You may have heard of the “fight or flight response.” When something potentially dangerous happens—for example, a speeding car, aimed right at you, appears out of nowhere—specialized areas of your brain respond by pumping out hormones that raise your heart rate, send extra blood to your muscles, and otherwise get you ready to fight—or run—for your life. This is only supposed to happen occasionally, when real danger arises. But chronic pain changes the behavior of the specialized “fight or flight” area of the brain, called the hypothalamus-pituitary-adrenal axis. The adrenaline level rises, and as the stress response continues, so does the level of cortisol, the body’s major stress hormone. That’s why Heather feels like she’s “on edge” so often; her body is constantly preparing her to fight or run for her life, even when there’s no danger.

These alterations to Heather’s brain are frightening enough. But there are others, including changes to some of the higher processing centers like the anterior cingulate cortex (ACC). The ACC is involved in a variety of cognitive and emotional functions. It helps us decide which actions to take and how we feel about situations and people. The ACC plays a key role in reward mechanisms, impulse control, decision making, and empathy. Indeed, studies on lesions (“wounds”) to the ACC show they create drastic personality changes. We know that the ACC goes through significant neuroplastic changes with chronic pain, and imaging studies indicate that it is a key center of activity for the “pain brain.” So it stands to reason that the way pain impacts the ACC can have a major influence on what we eat, how much alcohol we drink, our attitudes at any given moment, and whether or not we say “good morning” to people on the street.

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